Replacing carbohydrate with protein from meat, poultry, and dairy foods has beneficial metabolic effects and no adverse effects on markers of bone turnover or calcium excretion.

OBJECTIVE -To determine the effect of a high-protein (HP) weight loss diet compared with a lower-protein (LP) diet on fat and lean tissue and fasting and postprandial glucose and insulin concentrations.RESEARCH DESIGN AND METHODS -Replacing dietary protein for carbohydrate (CHO) during energy restriction and weight loss has been effective in sparing lean mass and improving insulin sensitivity in obese subjects but has not been tested in subjects with type 2 diabetes. We compared an HP diet (28% protein, 42% CHO, 28% fat [8% saturated fatty acids, 12% monounsaturated fatty acids, 5% polyunsaturated fatty acids]) with an LP diet (16% protein, 55% CHO, 26% fat [8% saturated fatty acids, 11% monounsaturated fatty acids, 5% polyunsaturated fatty acids]) in 54 obese men and women with type 2 diabetes during 8 weeks of energy restriction (1,600 kcal) and 4 weeks of energy balance. Body composition was determined by dual-energy X-ray absorptiometry at weeks 0 and 12.RESULTS -Overall, weight loss of 5.2 Ϯ 1.8 kg was achieved independently of diet composition. However, women on the HP diet lost significantly more total (5.3 vs. 2.8 kg, P ϭ 0.009) and abdominal (1.3 vs. 0.7 kg, P ϭ 0.006) fat compared with the women on the LP diet, whereas, in men, there was no difference in fat loss between diets (3.9 vs. 5.1 kg). Total lean mass decreased in all subjects independently of diet composition. LDL cholesterol reduction was significantly greater on the HP diet (5.7%) than on the LP diet (2.7%) (P Ͻ 0.01).CONCLUSIONS -Both dietary patterns resulted in improvements in the cardiovascular disease (CVD) risk profile as a consequence of weight loss. However, the greater reductions in total and abdominal fat mass in women and greater LDL cholesterol reduction observed in both sexes on the HP diet suggest that it is a valid diet choice for reducing CVD risk in type 2 diabetes. Diabetes Care 25:425-430, 2002T ype 2 diabetes is a major public health problem in the developed world (1). Although there is a strong genetic predisposition to the development of type 2 diabetes, lifestyle and dietary factors, particularly those that promote obesity, are contributors (2). Type 2 diabetes is characterized in most subjects by insulin resistance with inadequate insulin response to maintain normoglycemia (3). Insulin resistance occurs partly as a result of increased concentrations of circulating plasma free fatty acids, released from excess adipocytes in obesity, which compete with glucose for uptake in skeletal muscle (4). In addition, hormones such as resistin (5) and cytokines such as tumor necrosis factor-␣ (6) released from adipocytes may exacerbate insulin resistance. Because ϳ90% of people with type 2 diabetes are obese, weight loss is essential in management. The optimal diet for type 2 diabetes has been the focus of much research, and there remains no consensus on macronutrient composition apart from recommendations that saturated fats be kept low (7). Energy restriction alone significantly improves glucose control and the plasma lipid pro...

OBJECTIVE:To compare the long-term compliance and effects of two low-fat diets differing in carbohydrate to protein ratio on body composition and biomarkers of cardiovascular disease risk in obese subjects with hyperinsulinemia. DESIGN: Outpatient, parallel, clinical intervention study of two groups of subjects randomly assigned to either a standard protein (SP; 15% protein, 55% carbohydrate) or high-protein (HP; 30% protein, 40% carbohydrate) diet, during 12 weeks of energy restriction (B6.5 MJ/day) and 4 weeks of energy balance (B8.3 MJ/day). Subsequently, subjects were asked to maintain the same dietary pattern for the succeeding 52 weeks with minimal professional support. SUBJECTS: A total of 58 obese, nondietetic subjects with hyperinsulinemia (13 males/45 females, mean age 50.2 y, mean body mass index (BMI) 34.0 kg/m 2 , mean fasting insulin 17.8 mU/l) participated in the study. MEASUREMENTS: Body composition, blood pressure, blood lipids, fasting glucose, insulin, CRP and sICAM-1 were measured at baseline and at weeks 16 and 68. Urinary urea/creatinine ratio was measured at baseline, week 16 and at 3 monthly intervals thereafter. RESULTS: In total, 43 subjects completed the study with similar dropouts in each group (P ¼ 0.76). At week 68, there was net weight loss (SP À2.973.6%, HP À4.175.8%; Po0.01) due entirely to fat loss (Po0.001) with no diet effect. Both diets significantly increased HDL cholesterol concentrations (Po0.001) and decreased fasting insulin, insulin resistance, sICAM-1 and CRP levels (Po0.05). Protein intake was significantly greater in HP during the initial 16 weeks (Po0.001), but decreased in HP and increased in SP during 52-week follow-up, with no difference between groups at week 68, indicating poor long-term dietary adherence behaviour to both dietary patterns. CONCLUSION: Without active ongoing dietary advice, adherence to dietary intervention is poor. Nonetheless, both dietary patterns achieved net weight loss and improvements in cardiovascular risk factors.

Polycystic ovary syndrome (PCOS) is a common endocrine condition in women of reproductive age associated with obesity. It may involve dysregulation of ghrelin, a hormone implicated in appetite regulation. The effect of diet composition on ghrelin is unclear. Overweight women with and without PCOS were randomized to a high-protein (40% carbohydrate, 30% protein; 10 PCOS, six non-PCOS) or standard protein diet (55% carbohydrate, 15% protein; 10 PCOS, six non-PCOS) for 12 wk of energy restriction and 4 wk of weight maintenance. Diet composition had no effect on fasting or postprandial ghrelin or measures of satiety. Non-PCOS subjects had a 70% higher fasting baseline ghrelin (P = 0.011), greater increase in fasting ghrelin (57.5 vs. 34.0%, P = 0.033), and greater maximal decrease in postprandial ghrelin after weight loss (-144.1 +/- 58.4 vs. -28.9 +/- 14.2 pg/ml, P = 0.02) than subjects with PCOS. Subjects with PCOS were less satiated (P = 0.001) and more hungry (P = 0.007) after a test meal at wk 0 and 16 than subjects without PCOS. Appetite regulation, as measured by subjective short-term hunger and satiety and ghrelin homeostasis, may be impaired in PCOS.